gld-1, a Tumor Suppressor Gene Required for Oocyte Development in Caenorhabditis elegans

INVESTIGATIONS

gld-1, a Tumor Suppressor Gene Required for Oocyte Development in Caenorhabditis elegans

R. Francis, M. K. Barton, J. Kimble and T. Schedl
Department of Genetics, Washington University School of Medicine, St. Louis, Missouri 63110

We have characterized 31 mutations in the gld-1 (defective in germline development) gene of Caenorhabditis elegans. In gld-1(null) hermaphrodites, oogenesis is abolished and a germline tumor forms where oocyte development would normally occur. By contrast, gld-1(null) males are unaffected. The hermaphrodite germline tumor appears to derive from germ cells that enter the meiotic pathway normally but then exit pachytene and return to the mitotic cycle. Certain gld-1 partial loss-of-function mutations also abolish oogenesis, but germ cells arrest in pachytene rather than returning to mitosis. Our results indicate that gld-1 is a tumor suppressor gene required for oocyte development. The tumorous phenotype suggests that gld-1(+) may function to negatively regulate proliferation during meiotic prophase and/or act to direct progression through meiotic prophase. We also show that gld-1(+) has an additional nonessential role in germline sex determination: promotion of hermaphrodite spermatogenesis. This function of gld-1 is inferred from a haplo-insufficient phenotype and from the properties of gain-of-function gld-1 mutations that cause alterations in the sexual identity of germ cells.

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				M. P. Paronetto, F. Zalfa, F. Botti, R. Geremia, C. Bagni, and C. Sette The Nuclear RNA-binding Protein Sam68 Translocates to the Cytoplasm and Associates with the Polysomes in Mouse Spermatocytes Mol. Biol. Cell, January 1, 2006; 17(1): 14 - 24. [Abstract] [Full Text] [PDF]

				R. M. Zayas, A. Hernandez, B. Habermann, Y. Wang, J. M. Stary, and P. A. Newmark The planarian Schmidtea mediterranea as a model for epigenetic germ cell specification: Analysis of ESTs from the hermaphroditic strain PNAS, December 20, 2005; 102(51): 18491 - 18496. [Abstract] [Full Text] [PDF]

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